Targeting the CD40-CD154 Signaling Pathway for Treatment of Autoimmune Arthritis
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Critical Contribution of OX40 Ligand to T Helper Cell Type 2
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by PubMed Central Brief Definitive Report Critical Contribution of OX40 Ligand to T Helper Cell Type 2 Differentiation in Experimental Leishmaniasis By Hisaya Akiba,*§ Yasushi Miyahira,‡ Machiko Atsuta,*§ Kazuyoshi Takeda,*§ Chiyoko Nohara,* Toshiro Futagawa,* Hironori Matsuda,* Takashi Aoki,‡ Hideo Yagita,*§ and Ko Okumura*§ From the *Department of Immunology and the ‡Department of Parasitology, Juntendo University School of Medicine, Tokyo 113-8421, Japan; and §CREST (Core Research for Evolutional Science and Technology) of Japan Science and Technology Corporation, Tokyo 101-0062, Japan Abstract Infection of inbred mouse strains with Leishmania major is a well characterized model for analy- sis of T helper (Th)1 and Th2 cell development in vivo. In this study, to address the role of co- stimulatory molecules CD27, CD30, 4-1BB, and OX40, which belong to the tumor necrosis factor receptor superfamily, in the development of Th1 and Th2 cells in vivo, we administered monoclonal antibody (mAb) against their ligands, CD70, CD30 ligand (L), 4-1BBL, and OX40L, to mice infected with L. major. Whereas anti-CD70, anti-CD30L, and anti–4-1BBL mAb ex- hibited no effect in either susceptible BALB/c or resistant C57BL/6 mice, the administration of anti-OX40L mAb abrogated progressive disease in BALB/c mice. Flow cytometric analysis indicated that OX40 was expressed on CD41 T cells and OX40L was expressed on CD11c1 dendritic cells in the popliteal lymph nodes of L. major–infected BALB/c mice. In vitro stimu- lation of these CD41 T cells showed that anti-OX40L mAb treatment resulted in substantially reduced production of Th2 cytokines. -
A Fratricide-Resistant Allogeneic CAR T
Investigation of ALLO-316: A Fratricide- Resistant Allogeneic CAR T Targeting CD70 As a Potential Therapy for the Treatment of AML Surabhi Srinivasan, Nguyen Tan, Hsin-Yuan Cheng, Yi Zhang, Silvia Tacheva-Grigorova, Tom Van Blarcom, Cesar Sommer, Duy Nguyen , Barbra Sasu, and Siler Panowski 1 Disclosures • Full-time employee of Allogene Therapeutics • Equity interest in Allogene Therapeutics ALLO-316 (CD70) utilizes TALEN® gene-editing technology pioneered and owned by Cellectis. Allogene has an exclusive license to the Cellectis technology for allogeneic products directed at this target and holds all global development and commercial rights for this investigational candidate. 22 CONFIDENTIAL Disclaimers This presentation is not intended for product promotion. All information is related to investigational therapies not available for commercial use. The safety and efficacy of the therapies have not been established for FDA approval. Forward-Looking Statements To the extent statements contained in this Presentation are not descriptions of historical facts regarding Allogene Therapeutics, Inc. (“Allogene,” “we,” “us,” or “our”), they are forward-looking statements reflecting management’s current beliefs and expectations. Forward-looking statements are subject to known and unknown risks, uncertainties, and other factors that may cause our or our industry’s actual results, levels or activity, performance, or achievements to be materially different from those anticipated by such statements. You can identify forward-looking statements by words such as “anticipate,” “believe,” “could,” “estimate,” “expect,” “intend,” “may,” “plan,” “potential,” “predict,” “project,” “should,” “will,” “would” or the negative of those terms, and similar expressions that convey uncertainty of future events or outcomes. Forward-looking statements contained in this Presentation include, but are not limited to, statements regarding: the ability to progress the clinical development of allogeneic CAR T (AlloCAR T™) therapies and the potential benefits of AlloCAR T™ therapy, including ALLO-316. -
RANKL As a Novel EMT Marker 858 Cell Research (2008) 18:858-870
npg RANKL as a novel EMT marker 858 Cell Research (2008) 18:858-870. npg © 2008 IBCB, SIBS, CAS All rights reserved 1001-0602/08 $ 30.00 ORIGINAL ARTICLE www.nature.com/cr Receptor activator of NF-κB Ligand (RANKL) expression is associated with epithelial to mesenchymal transition in human prostate cancer cells Valerie A Odero-Marah1, Ruoxiang Wang1, Gina Chu1, Majd Zayzafoon2, Jianchun Xu1, Chunmeng Shi1, Fray F Marshall1, Haiyen E Zhau1, Leland WK Chung1 1Molecular Urology and Therapeutics Program, Department of Urology and Winship Cancer Institute, Emory University School of Medicine, 1365B Clifton Road, NE, Atlanta, GA 30322, USA; 2Department of Pathology, University of Alabamn, Birmingham, AL 35294, USA Epithelial-mesenchymal transition (EMT) in cancer describes the phenotypic and behavioral changes of cancer cells from indolent to virulent forms with increased migratory, invasive and metastatic potential. EMT can be induced by soluble proteins like transforming growth factor β1 (TGFβ1) and transcription factors including Snail and Slug. We uti- lized the ARCaPE/ARCaPM prostate cancer progression model and LNCaP clones stably overexpressing Snail to identify novel markers associated with EMT. Compared to ARCaPE cells, the highly tumorigenic mesenchymal ARCaPM and ARCaPM1 variant cells displayed a higher incidence of bone metastasis after intracardiac administration in SCID mice. ARCaPM and ARCaPM1 expressed mesenchymal stromal markers of vimentin and N-cadherin in addition to elevated levels of Receptor Activator of NF-κB Ligand (RANKL). We observed that both epidermal growth factor (EGF) plus TGFβ1 treatment and Snail overexpression induced EMT in ARCaPE and LNCaP cells, and EMT was associated with increased expression of RANKL protein. -
TNF Decoy Receptors Encoded by Poxviruses
pathogens Review TNF Decoy Receptors Encoded by Poxviruses Francisco Javier Alvarez-de Miranda † , Isabel Alonso-Sánchez † , Antonio Alcamí and Bruno Hernaez * Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Campus de Cantoblanco, Universidad Autónoma de Madrid, Nicolás Cabrera 1, 28049 Madrid, Spain; [email protected] (F.J.A.-d.M.); [email protected] (I.A.-S.); [email protected] (A.A.) * Correspondence: [email protected]; Tel.: +34-911-196-4590 † These authors contributed equally. Abstract: Tumour necrosis factor (TNF) is an inflammatory cytokine produced in response to viral infections that promotes the recruitment and activation of leukocytes to sites of infection. This TNF- based host response is essential to limit virus spreading, thus poxviruses have evolutionarily adopted diverse molecular mechanisms to counteract TNF antiviral action. These include the expression of poxvirus-encoded soluble receptors or proteins able to bind and neutralize TNF and other members of the TNF ligand superfamily, acting as decoy receptors. This article reviews in detail the various TNF decoy receptors identified to date in the genomes from different poxvirus species, with a special focus on their impact on poxvirus pathogenesis and their potential use as therapeutic molecules. Keywords: poxvirus; immune evasion; tumour necrosis factor; tumour necrosis factor receptors; lymphotoxin; inflammation; cytokines; secreted decoy receptors; vaccinia virus; ectromelia virus; cowpox virus Citation: Alvarez-de Miranda, F.J.; Alonso-Sánchez, I.; Alcamí, A.; 1. TNF Biology Hernaez, B. TNF Decoy Receptors TNF is a potent pro-inflammatory cytokine with a broad range of biological effects, Encoded by Poxviruses. Pathogens ranging from the activation of inflammatory gene programs to cell differentiation or 2021, 10, 1065. -
Dimerization of Ltβr by Ltα1β2 Is Necessary and Sufficient for Signal
Dimerization of LTβRbyLTα1β2 is necessary and sufficient for signal transduction Jawahar Sudhamsua,1, JianPing Yina,1, Eugene Y. Chiangb, Melissa A. Starovasnika, Jane L. Groganb,2, and Sarah G. Hymowitza,2 Departments of aStructural Biology and bImmunology, Genentech, Inc., South San Francisco, CA 94080 Edited by K. Christopher Garcia, Stanford University, Stanford, CA, and approved October 24, 2013 (received for review June 6, 2013) Homotrimeric TNF superfamily ligands signal by inducing trimers survival in a xenogeneic human T-cell–dependent mouse model of of their cognate receptors. As a biologically active heterotrimer, graft-versus-host disease (GVHD) (11). Lymphotoxin(LT)α1β2 is unique in the TNF superfamily. How the TNFRSF members are typically activated by TNFSF-induced three unique potential receptor-binding interfaces in LTα1β2 trig- trimerization or higher order oligomerization, resulting in initiation ger signaling via LTβ Receptor (LTβR) resulting in lymphoid organ- of intracellular signaling processes including the canonical and ogenesis and propagation of inflammatory signals is poorly noncanonical NF-κB pathways (2, 3). Ligand–receptor interactions α β understood. Here we show that LT 1 2 possesses two binding induce higher order assemblies formed between adaptor motifs in sites for LTβR with distinct affinities and that dimerization of LTβR the cytoplasmic regions of the receptors such as death domains or α β fi by LT 1 2 is necessary and suf cient for signal transduction. The TRAF-binding motifs and downstream signaling components such α β β crystal structure of a complex formed by LT 1 2,LT R, and the fab as Fas-associated protein with death domain (FADD), TNFR1- fragment of an antibody that blocks LTβR activation reveals the associated protein with death domain (TRADD), and TNFR-as- lower affinity receptor-binding site. -
RANK Interaction and Signaling − RANKL Structural and Functional
Structural and Functional Insights of RANKL −RANK Interaction and Signaling Changzhen Liu, Thomas S. Walter, Peng Huang, Shiqian Zhang, Xuekai Zhu, Ying Wu, Lucy R. Wedderburn, Peifu This information is current as Tang, Raymond J. Owens, David I. Stuart, Jingshan Ren and of October 1, 2021. Bin Gao J Immunol published online 14 May 2010 http://www.jimmunol.org/content/early/2010/05/14/jimmun ol.0904033 Downloaded from Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: by guest on October 1, 2021 http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Published May 14, 2010, doi:10.4049/jimmunol.0904033 The Journal of Immunology Structural and Functional Insights of RANKL–RANK Interaction and Signaling Changzhen Liu,*,†,1 Thomas S. Walter,‡,1 Peng Huang,x Shiqian Zhang,{ Xuekai Zhu,*,† Ying Wu,*,† Lucy R. Wedderburn,‖ Peifu Tang,x Raymond J. Owens,‡ David I. Stuart,‡ Jingshan Ren,‡ and Bin Gao*,†,‖ Bone remodeling involves bone resorption by osteoclasts and synthesis by osteoblasts and is tightly regulated by the receptor activator of the NF-kB ligand (RANKL)/receptor activator of the NF-kB (RANK)/osteoprotegerin molecular triad. -
The Unexpected Role of Lymphotoxin Β Receptor Signaling
Oncogene (2010) 29, 5006–5018 & 2010 Macmillan Publishers Limited All rights reserved 0950-9232/10 www.nature.com/onc REVIEW The unexpected role of lymphotoxin b receptor signaling in carcinogenesis: from lymphoid tissue formation to liver and prostate cancer development MJ Wolf1, GM Seleznik1, N Zeller1,3 and M Heikenwalder1,2 1Department of Pathology, Institute of Neuropathology, University Hospital Zurich, Zurich, Switzerland and 2Institute of Virology, Technische Universita¨tMu¨nchen/Helmholtz Zentrum Mu¨nchen, Munich, Germany The cytokines lymphotoxin (LT) a, b and their receptor genesis. Consequently, the inflammatory microenviron- (LTbR) belong to the tumor necrosis factor (TNF) super- ment was added as the seventh hallmark of cancer family, whose founder—TNFa—was initially discovered (Hanahan and Weinberg, 2000; Colotta et al., 2009). due to its tumor necrotizing activity. LTbR signaling This was ultimately the result of more than 100 years of serves pleiotropic functions including the control of research—indeed—the first observation that tumors lymphoid organ development, support of efficient immune often arise at sites of inflammation was initially reported responses against pathogens due to maintenance of intact in the nineteenth century by Virchow (Balkwill and lymphoid structures, induction of tertiary lymphoid organs, Mantovani, 2001). Today, understanding the underlying liver regeneration or control of lipid homeostasis. Signal- mechanisms of why immune cells can be pro- or anti- ing through LTbR comprises the noncanonical/canonical carcinogenic in different types of tumors and which nuclear factor-jB (NF-jB) pathways thus inducing cellular and molecular inflammatory mediators (for chemokine, cytokine or adhesion molecule expression, cell example, macrophages, lymphocytes, chemokines or proliferation and cell survival. -
Uva-DARE (Digital Academic Repository)
UvA-DARE (Digital Academic Repository) Balancing effector lymphocyte formation via CD27-CD70 interactions Arens, R. Publication date 2003 Link to publication Citation for published version (APA): Arens, R. (2003). Balancing effector lymphocyte formation via CD27-CD70 interactions. General rights It is not permitted to download or to forward/distribute the text or part of it without the consent of the author(s) and/or copyright holder(s), other than for strictly personal, individual use, unless the work is under an open content license (like Creative Commons). Disclaimer/Complaints regulations If you believe that digital publication of certain material infringes any of your rights or (privacy) interests, please let the Library know, stating your reasons. In case of a legitimate complaint, the Library will make the material inaccessible and/or remove it from the website. Please Ask the Library: https://uba.uva.nl/en/contact, or a letter to: Library of the University of Amsterdam, Secretariat, Singel 425, 1012 WP Amsterdam, The Netherlands. You will be contacted as soon as possible. UvA-DARE is a service provided by the library of the University of Amsterdam (https://dare.uva.nl) Download date:27 Sep 2021 Chapter 3 Constitutive CD27/CD70 interaction induces expansion of effector-type T cells and results in IFNy-mediated B cell depletion Ramon Arens*, Kiki Tesselaar*, Paul A. Baars, Gijs M.W. van Schijndel, Jenny Hendriks, Steven T. Pals, Paul Krimpenfort, Jannie Borst, Marinus H.J. van Oers, and René A.W. van Lier 'These authors contributed equally to this work Immunity 15, 801-812 (2001) Chapter 3 Constitutive CD27/CD70 interaction induces expansion of effector-type T cells and results in IFNy-mediated B cell depletion Ramon Arens123#, Kiki Tesselaar23", Paul A. -
TRAIL and Cardiovascular Disease—A Risk Factor Or Risk Marker: a Systematic Review
Journal of Clinical Medicine Review TRAIL and Cardiovascular Disease—A Risk Factor or Risk Marker: A Systematic Review Katarzyna Kakareko 1,* , Alicja Rydzewska-Rosołowska 1 , Edyta Zbroch 2 and Tomasz Hryszko 1 1 2nd Department of Nephrology and Hypertension with Dialysis Unit, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] (A.R.-R.); [email protected] (T.H.) 2 Department of Internal Medicine and Hypertension, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] * Correspondence: [email protected] Abstract: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a pro-apoptotic protein showing broad biological functions. Data from animal studies indicate that TRAIL may possibly contribute to the pathophysiology of cardiomyopathy, atherosclerosis, ischemic stroke and abdomi- nal aortic aneurysm. It has been also suggested that TRAIL might be useful in cardiovascular risk stratification. This systematic review aimed to evaluate whether TRAIL is a risk factor or risk marker in cardiovascular diseases (CVDs) focusing on major adverse cardiovascular events. Two databases (PubMed and Cochrane Library) were searched until December 2020 without a year limit in accor- dance to the PRISMA guidelines. A total of 63 eligible original studies were identified and included in our systematic review. Studies suggest an important role of TRAIL in disorders such as heart failure, myocardial infarction, atrial fibrillation, ischemic stroke, peripheral artery disease, and pul- monary and gestational hypertension. Most evidence associates reduced TRAIL levels and increased TRAIL-R2 concentration with all-cause mortality in patients with CVDs. It is, however, unclear Citation: Kakareko, K.; whether low TRAIL levels should be considered as a risk factor rather than a risk marker of CVDs. -
Targeting the Lymphotoxin-B Receptor with Agonist Antibodies As a Potential Cancer Therapy
Research Article Targeting the Lymphotoxin-B Receptor with Agonist Antibodies as a Potential Cancer Therapy Matvey Lukashev,1 Doreen LePage,1 Cheryl Wilson,1 Ve´ronique Bailly,1 Ellen Garber,1 AlexLukashin, 1 Apinya Ngam-ek,1 Weike Zeng,1 Norman Allaire,1 Steve Perrin,1 Xianghong Xu,1 Kendall Szeliga,1 Kathleen Wortham,1 Rebecca Kelly,1 Cindy Bottiglio,1 Jane Ding,1 Linda Griffith,1 Glenna Heaney,1 Erika Silverio,1 William Yang,1 Matt Jarpe,1 Stephen Fawell,1 Mitchell Reff,1 Amie Carmillo,1 Konrad Miatkowski,1 Joseph Amatucci,1 Thomas Crowell,1 Holly Prentice,1 Werner Meier, 1 Shelia M. Violette,1 Fabienne Mackay,1 Dajun Yang,2 Robert Hoffman,3 and Jeffrey L. Browning1 1Departments of Immunobiology, Oncopharmacology, Molecular Engineering, Molecular Profiling, Molecular Discovery, Antibody Humanization, and Cellular Engineering, Biogen Idec, Cambridge, Massachusetts; 2Division of Hematology and Oncology, University of Michigan, Ann Arbor, Michigan; and 3AntiCancer, Inc., San Diego, California Abstract receptor (TRAILR) 1/2, death receptor (DR) 3, DR6, and possibly ectodermal dysplasia receptor (EDAR). These TNFRs harbor The lymphotoxin-B receptor (LTBR) is a tumor necrosis factor signaling adaptor motifs termed death domains that can initiate receptor family member critical for the development and the extrinsic apoptosis program. In addition, TNFRs of this group maintenance of various lymphoid microenvironments. Herein, can exert antitumor effects via other mechanisms that include we show that agonistic anti-LTBR monoclonal antibody (mAb) tumor sensitization to chemotherapeutic agents, activation of CBE11 inhibited tumor growth in xenograft models and antitumor immunity, and disruption of tumor-associated micro- potentiated tumor responses to chemotherapeutic agents. -
Increased Expression of CD154 and FAS in SLE Patients’ Lymphocytes Maria Elena Manea, Ruediger B
Increased expression of CD154 and FAS in SLE patients’ lymphocytes Maria Elena Manea, Ruediger B. Mueller, Doru Dejica, Ahmed Sheriff, Georg Schett, Martin Herrmann, Peter Kern To cite this version: Maria Elena Manea, Ruediger B. Mueller, Doru Dejica, Ahmed Sheriff, Georg Schett, et al.. Increased expression of CD154 and FAS in SLE patients’ lymphocytes. Rheumatology International, Springer Verlag, 2009, 30 (2), pp.181-185. 10.1007/s00296-009-0933-4. hal-00568285 HAL Id: hal-00568285 https://hal.archives-ouvertes.fr/hal-00568285 Submitted on 23 Feb 2011 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Increased expression of CD154 and FAS in SLE patients’ lymphocytes Maria Elena Manea1‡, MD, Ruediger B. Mueller2,3‡, MD, Doru Dejica1, PhD, Ahmed Sheriff2, PhD, Georg Schett2, MD, Martin Herrmann2, PhD, Peter Kern4, MD 1 Department of Immunopathology. “Iuliu Hatieganu" University of Medicine and Pharmacy, Str Croitorilor no 19-21, 3400 Cluj-Napoca, Romania. 2 Department for Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen-Nürnberg, Germany 3 Departement of Rheumatologie, Kantonsspital St. Gallen, Switzerland 4 Franz von Prümmer Klinik, Bahnhofstraße 16, 97769 Bad Brückenau, Germany ‡ both authors equally contributed to the work Address correspondence and reprint requests to: Ruediger B. -
Cell-Expressed CD154 in Germinal Centers Expression, Regulation
Expression, Regulation, and Function of B Cell-Expressed CD154 in Germinal Centers Amrie C. Grammer, Richard D. McFarland, Jonathan Heaney, Bonnie F. Darnell and Peter E. Lipsky This information is current as of September 25, 2021. J Immunol 1999; 163:4150-4159; ; http://www.jimmunol.org/content/163/8/4150 Downloaded from References This article cites 74 articles, 33 of which you can access for free at: http://www.jimmunol.org/content/163/8/4150.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 25, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 1999 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Expression, Regulation, and Function of B Cell-Expressed CD154 in Germinal Centers1 Amrie C. Grammer,* Richard D. McFarland,† Jonathan Heaney,* Bonnie F. Darnell,† and Peter E. Lipsky2* Activated B cells and T cells express CD154/CD40 ligand in vitro. The in vivo expression and function of B cell CD154 remain unclear and therefore were examined.